文献类型：期刊文献

中文题名：黄芪对矽肺大鼠肺组织胶原合成的影响

英文题名：Effects of astragalus and astragalus extract on collagen synthesis in rat lungs exposed to silica

作者：陈丽[1];颜春鲁[1];赵翊[1];岳嘉[1];慕婷婷[1];张书楠[1]

第一作者：陈丽

机构：[1]甘肃中医药大学,甘肃兰州730000

第一机构：甘肃中医药大学

年份：2017

卷号：43

期号：5

起止页码：359

中文期刊名：工业卫生与职业病

外文期刊名：Industrial Health and Occupational Diseases

收录：CSTPCD

基金：敦煌医学与转化省部共建教育部重点实验室开放基金(DHYX1213-002);甘肃省教育厅第二批科研项目计划(1106B-05);甘肃中医学院中青年基金项(BH2011-0020)

语种：中文

中文关键词：黄芪;矽肺;胶原蛋白;超氧化物歧化酶;丙二醛

外文关键词：Astragalus; Silicosis; Collagen;Superoxide dismutase; Malondialdehyde

摘要：目的研究黄芪及其提取物对矽肺大鼠肺组织胶原合成的抑制作用及其对抗氧化物酶活力和脂质过氧化水平的影响。方法将SPF级Wistar雄性大鼠124只随机分为正常组、模型组、乙酰半胱氨酸组、黄芪水煎液组、黄芪总苷组、黄芪多糖组,每组24只。大鼠氯胺酮麻醉后,采用经气管染SiO_2粉尘法复制矽肺模型。干预组注入SiO_2粉尘后1d开始灌胃,正常组及模型组给予等体积的生理盐水灌胃。观察各组肺组织病理改变,采用羟脯氨酸(Hyp)测定法对各组大鼠肺内胶原含量进行检测,分别采用硫代巴比妥酸法、黄嘿吟氧化酶法测肺内丙二醛(MDA)含量及超氧化物歧化酶(SOD)活力。结果第28天,各干预组与模型组比较,病理形态改变有不同程度的减轻,各干预组Hyp均明显低于模型组(P<0.05),SOD活力各干预组与模型组比较均有所升高,其中第14天和第28天各干预组模型组比较,差异有统计学意义(P<0.05),MDA含量第14天乙酰半胱氨酸组和黄芪水煎液组与同时期模型组比较明显下降(P<0.05),各干预组第28天与模型组比较,差异均有统计学意义(P<0.05)。结论黄芪、黄芪多糖、黄芪总苷均能够降低矽肺大鼠肺内胶原蛋白含量,对矽肺纤维化有抑制作用,可能与其提高抗氧化物酶SOD的活力、减轻脂质过氧化损伤,提高机体的抗氧化损伤能力有关。
Objective To explore the effects of Astragalus and Astragalus extract on the collagen synthesis,antioxidase activities,and levels of lipid peroxidation in silicotic rats. Methods Aninal model was established by direct tracheal instillation of silica into rat lungs through tracheostmy. After tracheotomy these rat were divided into six groups： control group, model group,huangqi decoction liquid group, total glycosides group,astragalus polysaccharide group, acetyl cysteamine acid group. After 1 weeks. 2 weeks and4 weeks the animals were killed and histopathological test was performed on the lung. The pathological changes of the lung tissue were observed by HE staining, and collagen contents were detected by Hydroxyproline（ Hyp）assay. The malondialdehyde（MDA）contents and superoxide,dismutase（SOD）activities in plasma were assayed by thibabituric acid method, and xanthine oxidase method, respectively. Results The rats＇ general physical condition significantly improved by the Astragalus. The pulmonary alveolitis and put-monary fibrosis degree reduced also. Hyp contents in the Astragalus treated groups were lower than in the silica group, MDA contents in the Astragalus treated group with high, medium doses were significantly lower than in the silica group. SOD activities in the Astragalus treated groups were significantly higher than in the silica group. Conclusions Astragalus could inhibit the synthesis of lung collagen and pulmonary fibrosis induced by silica. The possible antifibrotic mechanism of Astragalus is through increasing the activities of SOD and inhibiting lipid peroxidation.